Abstract


Introduction

Diabetes insipidus (DI) presents with hypernatremia and hyperosmolality in individuals with an impaired thirst mechanism1 or no free access to water. Hyperosmolality is associated with rhabdomyolisis, a disease consisting of elevated serum creatinine kinase (CPK) and myoglobinuria. Fluid resuscitation is the mainstay of the treatment to prevent life-threatening complications including acute hyperkalemia and acute kidney injury.
We present herein a first human case of nephrogenic DI who presented with rhabdomyolisis.

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Introduction

Diabetes insipidus (DI) presents with hypernatremia and hyperosmolality in individuals with an impaired thirst mechanism1 or no free access to water. Hyperosmolality is associated with rhabdomyolisis, a disease consisting of elevated serum creatinine kinase (CPK) and myoglobinuria. Fluid resuscitation is the mainstay of the treatment to prevent life-threatening complications including acute hyperkalemia and acute kidney injury.
We present herein a first human case of nephrogenic DI who presented with rhabdomyolisis.

Case presentation
A 74 year old man with multiple comorbidities along with an unknown type of DI was transferred to our hospital for fever and cough. He was in respiratory distress and lethargic. His vitals reported as a blood pressure of 127/49 mmHg and a heart rate of 101 beats per minute. Temperature was 104 F rectally. Respiratory rate was 29 per minute; oxygen (02) saturation was 88 % which improved to 92 % with supplemental 02. He had crackles on the left lung base and opacity over the same area on chest Xray. Fluid resuscitation with normal saline and empiric antibiotics started for the treatment of severe sepsis. Patient required continuous BiPAP and was kept nothing by mouth (NPO). His urine output was 10 L over first 24 h (n 800-2000 ml/24 h) and further diagnostic tests were obtained. Blood sugar was around 200 mg/dL and HbA1c was 6.1 %. Creatinine was 1.1 mg/dL (n 0.8-1.4 mg/dL) and serum electrolytes were sodium of 129 mEq/L (n 136-147 mEq/L), potassium of 4.5 mEq/L (n 3.6-5.2 mEq/L) and bicarbonate of 30 mEq/L (n 23-32 mEq/L). Urine studies showed specific gravity of 1.002 (n 1.005-1.030), sodium of 61 Mmol/L and potassium of 9 Mmol/L. Urine dipstick was positive for occult hematuria but RBCs were absent in urine samples. Urine drug screen was negative. In a repeat metabolic panel, serum sodium increased to 152 mEq/L along with serum osmolality of 363 uosm/kg (n 275-295 uosm/kg) and urine osmolality of 128 uosm/kg (n 300-900 uosm/kg). Despite switching to hypotonic maintenance fluid, serum sodium rose up to 170 mEq/L and persisted around the range of 160-170 mEq/L. Serum CPK was 1927 U/L (n 32-230 U/L) which trended up to 2240 U/L in contempt of normal kidney function. There was no history of trauma or fall or the use of statin or other drugs which induce rhabdomyolisis. Desmopressin was given with no significant response. He was diagnosed with nephrogenic DI, started on thiazide. Later he was weaned from BiPAP and allowed to eat and drink. Serum osmolality was back to 291 uosm/kg and CPK to 90 U/L.

Conclusion
Hypernatremia and hyperosmolality are significant predisposing factors for rhabdomyolysis2. Nephrogenic DI should be considered in differentials of non-traumatic rhabdomyolisis along with other hyperosmolar states including severe dehydration, diabetic nonketotic hyperosmolar coma and central DI. Serum CPK levels should be monitored closely to prevent complications.

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